Initially it was proposed monosodium urate crystals might initiate an inflammatory process associated with acute gouty arthritis by activating Hageman factor which in turn would initiate additional reactions resulting in the activation of kallikrein and the formation of kinins. These are potent inflammatory mediators capable of reproducing many of the characteristics of an acute inflammatory response. Although urate crystals indeed can activate Hageman factor and initiate the formation of kinins in synovial fluid it has not been proven that these agents play an important role in the initiation of acute gouty arthritis. Studies done with another animal model, namely the foreign body reaction associated with the deposition of the divinyl co-polymer benzene bead in the microvasculature of the mouse lung indicate that this inflammatory process is dependent, at least in large part, on the generation of these mediators. Studies of these inflammatory reactions are being pursued further. Specifically we are looking at the role of cholera toxin factor in these inflammatory processes at the present time.